Good morning and welcome to the Avacta Group PLC Investor Presentation. Throughout this recorded meeting, investors will be in listen-only mode. Questions can be submitted by the Q&A tab situated in the right-hand corner of your screen. Just simply type in your question and press send. The company will not be in a position to answer every question received during the meeting itself, and the company can view all questions submitted today and publish responses where it's appropriate to do so. Before we begin, we'd like to submit the following poll. I'd now like to hand you over to Christina Coughlin, CEO. Good morning. Thanks, Paul. Good morning, and thank you, everyone, for joining us for the data release for AVA6000 in Phase 1B in patients with salivary gland cancers. I'm joined today by two team members: our Chief Medical Officer, David Liebowitz, and our translational scientist for this program, Ruairidh Edwards. Let's dive right in. preCISION is a FAP-activated drug delivery program, which essentially renders a given toxic drug for oncology silent in the bloodstream and active in the tumor by the binding of the preCISION peptide to mask the toxic payload in the bloodstream and in the normal tissues. Drug release is then only triggered at the tumor site by FAP, fibroblast activation protein, a protein that's been found in tumor-supporting cells. The preCISION peptide masks the toxic effects of the drug in normal tissues and in the bloodstream, and that drug is then released actively in the tumor by virtue of Fibroblast Activation Protein, or FAP, cleaving the peptide and releasing the active drug. Because normal tissues and the bone marrow essentially are not exposed to the toxic effects to the degree that they would be with conventional drugs, this has enabled prolonged treatment beyond that permitted with conventional therapy, which then translates into enhanced survival. We're excited to bring you the enhanced survival that we have seen with the second cohort, the Phase 1B cohort. Preliminary data here that Dave will take you through. Just a quick reminder that the preCISION mechanism of action essentially leverages the bystander effect, whereby FAP cleaves the peptide from the peptide drug conjugate, releasing the active payload extracellularly, so outside of the cells, outside of the cancer-associated fibroblasts, then allowing the active drug to move into the FAP-negative tumor cells. Ruairidh will take you through some of the real patient data, looking at the level of FAP that is expressed in some of these tumors, some highly encouraging data that really speaks to the power of the preCISION platform. Essentially, in the Phase 1A component of the trial, we've made four key observations. The first is that AVA6000 has eliminated the severe cardiac toxicity that is associated with conventional doxorubicin. It has dramatically reduced the hematologic and the GI toxicities associated with conventional doxorubicin. We see a dramatic concentration of released doxorubicin in the tumor versus the plasma, which is the exact mechanism of action of the drug. And finally, we do see evidence of preliminary activity in both salivary gland cancers as well as soft tissue sarcoma. Both of these were presented at the European Society for Medical Oncology in September of this year. Encouraging activity, and Dave is going to take us through the updates now in the Phase 1B cohort. David. Thank you, Chris. Hi, I'm David Liebowitz, and I'm going to take you through the updated data with our Phase 1B information. So just a quick background on salivary gland cancers. They're pretty rare, with only 2,000 to about 2,500 cases per year in the United States. Importantly, there's no standard of care treatment regimen for patients with advanced disease, and a small subset of patients that are eligible for HER2-directed therapy or androgen deprivation therapy exists. But again, this is a small subset. So just to remind you, here's the AVA6000 Phase 1 trial design. You can see that the number of patients that were treated in 1A and then the rest of the patients were treated in 1B, which is 19 that I'm going to tell you about. Okay, so the baseline characteristics are listed here. A couple of notable features: the ECOG performance status was very good at zero to one, and the number of prior regimens down at the bottom of the slide with a median of two and a range of zero to two. The safety profile is similar to what we saw in the Phase 1A. There's a low incidence of Grade 3 or 4 neutropenia, which is notable. Most importantly, I think for this drug, there's no Grade 3 or 4 cardiac toxicities that have been observed. Here's an update to our waterfall plot. This has Phase 1A and Phase 1B patients. Notably, we have nine patients that had either partial or minor responses, and you see the 90% disease control rate that we've achieved in this population of patients. Here's the updated waterfall—I mean, sorry, swimmer plot. And what you can see here is that most of the patients are still ongoing, and we have not reached our median follow-up at this point. Okay, with that, I'll hand it over to Ruairidh to go through the translational data. Thanks, David. So we've had probably one of the largest datasets for salivary gland cancer that is out there in terms of translational analysis, and that's really exciting to us. And so we've leveraged that to not only provide us with data that can help us with the AVA6000 program, but also data that can help guide the AVA6103 program that is upcoming. So I want to take you through a couple of case studies from the Phase 1B cohort that Dave has already kind of outlined the excellent efficacy data that's been observed, as well as safety data. And this first case study here is of a 52-year-old male patient who was diagnosed with a subtype of salivary gland cancer called adenoid cystic carcinoma. And this was a high-grade cancer that was particularly differentiated, it's not very well differentiated, sorry, compared to the normal tissue. And so this patient had received surgery to remove the primary tumor, as well as radiotherapy for any localized disease. They hadn't received any systemic therapy, and to treat the disease that remained, they enrolled on the AVA6000 study in the Phase 1B, which is dosed at 310 milligrams per meter squared every three weeks. What's exciting is if we look at this plot on the bottom left-hand corner of this slide, what we're looking at here is immunofluorescence images from this patient. So this is a biopsy from the patient that they've kindly provided us. And what we've stained for is FAP expression in green, the tumor cells in aqua blue, and then the blood vessels in red. And what's really interesting when you look at this data is that you see this patient is FAP low. There is not a lot of FAP present within this patient's tissue. However, this patient has had a minor response. At the third week scan, we've had a minus 22.7% reduction in tumor lesions, which is fantastic to see. And that really kind of indicates that we don't need a lot of FAP in the tumor to drive an anti-tumor response. And that can be seen from these scan images just to the bottom right of the slide here. This is a baseline compared to the third six-week scan the patient has received. And so you can see that more than 20% reduction. So that's really exciting. That kind of suggests that not just for AVA6000, but for the precision platform as a whole, there's potential to go into low FAP indications and really expand the patient population which precision medicines can treat. I'll move on to our second case study. This case study is a little different. This patient is a 52-year-old female who was diagnosed with recurrent Adenoid Cystic Carcinoma. I believe this patient had metastatic disease. The patient, again, received surgery and radiotherapy to treat the local disease. However, they then enrolled on AVA6000 clinical study to treat the remaining disease. You'll see this quite common among salivary gland patients purely from the fact that there is no standard of care within this indication. There is no standard therapy that doctors go to to treat this cancer. When this patient enrolled on the AVA6000 study, they kindly provided again another tumor biopsy for us to analyze. This time, we're looking at a slightly different histology analysis. And this time, we're looking at what's called DAB staining, where, in brown, we're staining for the protein FAP. So again, this is just looking for FAP expression. And then, in blue, is the negative tumor cells that surround the FAP-positive cancer-associated fibroblasts. This patient has moderate to high FAP expression. You can see from the intensity of brown that's observed in that image in the middle there. And this is only a small, small portion of this patient's tumor. You can see on the left-hand side, that's the full extent of the biopsy, which is much larger and still contains lots of FAP. Now, this patient has so far had a minor response and has seen the minor response at their second scan. So this is encouraging to see. When we look at the scan data on the right there, we can see the reduction in target lesions that is observed. After the case studies, I wanted to kind of show you some of the data that we've generated from the population of salivary gland patients as a whole. This slide is basically showing a bar graph of the proportions of patients with negative, weak, moderate, or strong FAP expression. The negative are in gray, which are classed as 0. The 1 plus, which is the weak, that is shown in the dark blue. The 2 plus in the kind of lighter blue. Then 3 plus is in the teal, and that's strong FAP expression. What's really encouraging to see is that the majority of patients, first of all, are FAP-positive. I should mention that these patients are all from AVA6000 study participants. This is our real-world study data. You can see here that the majority of the patients on study have high FAP expression. If we class, we typically class a 2 plus or a 3 plus as high FAP expression. You can see that is about 70% of all patients on study. On the right here, I just have kind of illustrated examples of the histology data that we kind of observe that determines the scoring. This kind of gives you an idea of what a 0 plus looks like at the bottom here, a 1 plus, the next one up, and then so on and so forth for the 2 plus and 3 plus. You can see they gradually get more and more brown. The intensity of brown increases, and that again is just staining for FAP. It's good to see that this indication does tend to have FAP high patients come through the door. On top of that, we do know that even the FAP low patients do appear to respond. This is a very large patient population that we can potentially treat. This is a particularly interesting slide, and this is one of my favorite slides, actually, to be honest. The reason for that is because this data is incredibly precious to us. What we're looking at here is patients that have kindly provided fresh tumor biopsies on study. What they've done is after they've received the dose of AVA6000, they come into the clinic 24 hours post-dosing, and they provide us with a tumor biopsy. This biopsy is then analyzed for drug concentration levels, and then we can evaluate and compare the tumor drug concentration levels compared to the plasma. And in this case, what we're looking at is doxorubicin concentration. So we can see here on the graph that the tumor-to-plasma ratio for salivary gland cancer patients only, these are salivary gland cancer biopsies, is substantially higher. So there's far more in the tumor than there is in the plasma. And I've actually noted on the slide here something else which is quite interesting, and that is this line that runs across just below the 100 nanograms per gram of tissue marker there. This is depicting the amount of drug required to kill salivary gland cancer cells in vitro. And when I mean in vitro, I mean in cell culture in the lab. What they've done is they've tested doxorubicin and treated this cancer cell line with doxorubicin. Then they've essentially evaluated to see how much drug does it take to kill 90% of those salivary gland cancer cells. It comes out to just below 100. It's about 70, actually, nanograms per gram when converted into that particular metric. What's exciting to us is that we can see that all the biopsies sit higher than this concentration. In other words, all biopsies are receiving more drug, more doxorubicin to the tumor than is required to kill 90% of the salivary gland cancer cells in culture, in cell cultures. What's also quite exciting is if you look at the right-hand side of the graph and the arrows that point towards the histology, we're seeing that this accumulation of drug can happen at varying degrees of FAP expression. We can see that on the bottom panel there, the bottom histology image. This is a 2 plus image with some reasonable drug concentration, doxorubicin concentration in the tumor. In the middle, that middle graph, it has a 1 plus. So it's fairly weak FAP staining. This patient doesn't have a lot of FAP in the tumor. However, they have a very high concentration of drug in the tumor, one of the highest of all patients that have provided biopsies. And so this kind of gives us, again, an indication that we don't necessarily need a lot of FAP to really deliver doxorubicin to the tumor via AVA6000. And that makes it very exciting as a potential platform. And this is some data that really provides us with a strong proof of mechanism. So with that, I'll hand over to Chris. Thanks, Ruairidh. Thanks, Dave. Much appreciated. So the key takeaways from these data today, we are seeing that the safety profile of AVA6000 is consistent in the Phase 1B. This is incredibly encouraging. We see no cardiac toxicity. We see very dramatic reductions in the GI toxicities, the hematologic toxicities. The preliminary efficacy observed in the Phase 1B portion of the trial as well is also highly encouraging. We are seeing the same statistics. It wasn't a mistake what happened in phase 1. We're thrilled. 90% disease control rate holds up. That essentially tells us the number of or the percentage of patients that are seeing benefit from the drug. As Ruairidh described, the release of doxorubicin observed and the tumor shrinkage is noted even at very low levels of FAP. This is critically important both for the salivary gland indication, but also for the platform moving forward in that it does open up for us a number of diseases where we see FAP levels somewhat low in a subset of the patients. I'll give you a great example in the FAP exatecan or AVA6103. Small cell lung cancer is one of those disease settings where these data are really supportive of us taking that disease setting forward. We see released doxorubicin in the tumor at the levels, as Ruairidh described, that are able to hit that level of concentration that we need in order to kill those tumor cells. Again, solid proof of mechanism really showing how preCISION works. Finally, we do continue to enroll into the Phase 1B portion of the trial, and there will be further data updates. As Dave mentioned, there are some differences in the patient population. This group of patients has a median number of prior lines of therapy of one. There were seven patients treated in the first line setting in this patient population. And so we have moved slightly into an earlier phase setting with this patient population. We will continue to observe these patients. We continue to collect the survival endpoints, both progression-free survival as well as overall survival in this patient population. And with that, I'm going to turn it back over to Paul, and we will take some questions on the data. Fantastic, Chris. Thank you and the team for your presentation. As you can see, we received a number of questions both pre-submitted and throughout today's presentation. Thank you to all the investors for submitting those. As today is focused on the data, the management team will focus now on the questions regarding the data presented in today's data release. The team will not be able to, obviously, respond to all questions submitted in today's session, but Chris and the team will review those questions submitted. Okay, Chris, perhaps if I can start with the first question, it reads as follows. We've not reached median PFS in the Phase 1B cohort reported today. However, that's the key trial endpoint which you described for the next study. Can you describe what's needed to reach that endpoint? Yeah, good question. So this cohort of patients, the Phase 1B, these patients were treated sometime after the Phase 1A cohort. Very correct. And thus, it's going to take some time. It's going to take us a bit longer to collect the progression-free survival data and really determine in this group of patients what is the median there. As David described, most of the patients are actually still receiving drug, not even that most of them are in PFS follow-up, which is what we've seen at ESMO with the Phase 1A cohort. Now, with the current number of 19, we would need mathematically in this cohort 10 patients to progress in order to see the median. And again, most of the patients are still on drug. And so I don't think that we're going to see that median soon. If you think about it, we first reported the Phase 1A in April of last year at AACR, and then we were close to the median when we got to September. So it does take time. And also to note, importantly, that we do continue to enroll in this cohort, and as such, there will be additional patients. So more in this phase will significantly reduce the risk of taking the drug forward in that phase 2, 3 trial that we have discussed. Thanks, Chris. The next question we've got here, the development plan, as we see, includes the Phase 2/3 trial. Are there more details regarding this design of the trial or when it will start? How will this trial support an approval in this indication? Yes, the preliminary data here do support the design, so this trial is designed, and it's designed for a drug such as this one, which will use that progression-free survival endpoint. We're looking at that PFS as the primary endpoint that we can achieve here, and we think that we can achieve substantial positive outcomes here by looking at this endpoint. We've seen that in the Phase 1A, and even in this preliminary and early data cut from the Phase 1B, we're still looking at a 90% disease control rate, meaning 90% of the patients are seeing disease stabilization. Now, AVA6000 is not resulting in a high response rate with the two partial responses and the seven minor responses in these first two cohorts, but so we will utilize that endpoint of PFS. We will also utilize the endpoint of overall survival. Because it's a survival endpoint, we need to compare it to an investigator's choice of chemotherapy regimens. Now, this design is supported by the global guidelines. We've talked about this before. The global guidelines for the treatment of this disease show that there's no standard regimen that's used in either the first line or the second line setting. The current approval planning that we're working on involves a randomized Phase 2/3 trial to support potential approval here, as I mentioned. The next steps can be better planned out once we've collected the PFS in this second cohort. This gives us more than 30 patients to plan the statistics in that registration trial. We understand that the time needed here can be frustrating. However, the best next steps for us are to really collect this data, and that allows us to plan the trial. It allows us to specifically plan the statistics around the data collected. Those statistics then feed into the number of patients that will need to be treated in that trial to show an adequate statistical difference between the investigator's choice arm and the FAP doxorubicin arm. It likely goes without saying that we can't plan that larger registration trial on the 11 patients. And it's going to be important for us to understand, as Dave mentioned, that median number of prior lines being one and several of the patients in this cohort having no prior therapy. This is going to allow us to really predict what the efficacy will be in both the first line and the second line setting here. That's great. Thanks, Chris. Next question we've got here. There's 19 patients being reported. Will there be more, and why are we discussing 22 patients in some places? Good point. Good point. There are 19 patients in this cohort that are available for efficacy, and there are an additional three patients that were enrolled. And so importantly, to determine that a patient is available for efficacy outcomes, thus the 19 and not the 22, there's two factors. First, the patients must have met the inclusion and not the exclusion criteria to be eligible for the trial. And two, they must have had an efficacy evaluation. It's important in an ongoing study that we make sure the number of patients included that they have been assessed for efficacy, meaning they've had at least one scan, one follow-up scan. And so of those three patients that are not included in the efficacy outcomes, two of the 22 didn't meet eligibility. So they had an ECOG of two, and thus they're not included in the cohort. They weren't eligible for the trial, and there's one patient who was enrolled, treated with the first dose, but has not had an on-treatment scan, so they're not included here in the efficacy outcome, but they will be included in future updates. It's also important to note that when we looked at the safety analyses, these three patients are included because each of the three patients did receive at least one dose of the drug, so these patient sets, they're called analysis sets, and in an ongoing study like this, they can have different numbers, so we have an analysis set for efficacy, and we have an analysis set for safety. It's a good question. I'm glad to be able to provide that clarity. Thank you. Next one we've got here is, median PFS being reached in the Phase 1A cohort of 11 patients. This data cut will happen in October. So is there an update for this patient population when additional data will be available? Yes, we've not updated the data for the Phase 1A portion of the trial here. As this listener noted, the data cut-off here is in October, and that would have only been about an hour, about a month since the data cut-off. So it's very close to the ESMO meeting. Once we've collected further data in both of these cohorts, we will update those in the first half of 2026. And as we've noted before, the collection of the PFS data in both cohorts is going to give us a much larger number of patients than the 11 that we have in that Phase 1A. So we haven't updated that. So at this point, the most recent data cut that we have from that was ESMO, but we do expect to update the data in both of these cohorts in the first half of 2026. The collection of survival data in these cohorts does take a long time. We do understand that this can be a frustrating part of our business. However, these survival endpoints are really the most important in oncology trials. The data here are critical to de-risk our next stage of development and plan the statistics around that next trial. And so, this next statement that I'm going to make here: many phase 3 trials that have been reported in failures could have been averted by collecting more data prior to going to the larger registration trial. It really helps our statisticians to have a lot of confidence and a greater degree of confidence around their predictions of what we'll observe in that next trial. Thank you. How's the recruitment and patient experience in P1B? Wondering how patients are finding the drug. So good question. In any new cohort, recruitment can be quite slow at the beginning. It really can be. And then it picks up over time. And we see this with any new trial, with any new cohort. This is exactly what we see with the salivary gland cancer cohort. Many of the patients, as we saw in the waterfall and in the swimmer plot, are still on therapy. In the waterfall, it was the asterisks, and in the swimmer plot, it's the arrows. Some have not had enough time to even be evaluable for efficacy. So we do continue to enroll here, and the important point is that we continue to collect these data, and we continue to assess the patients in this cohort. Here we go. When can we expect the Phase 1B cohort and Phase 1A cohort to be read out for the Phase 2/3? As we understand the data from these cohorts, we'll plan the next stage of development. Yes, these data will be needed, as mentioned, to plan for that next Phase 2/3 trial. It will be a randomized study, likely randomized two to one, meaning every two patients receive AVA6000, one patient receives investigator's choice or the control arm. It's important for this trial, as we design it, that we utilize our current data to plan the statistics. It's frustrating that we know we have to wait for the survival endpoints for this arm, but what it does is it significantly de-risks the Phase 2/3 trial. We're very encouraged by the activity that we've already seen in both the first-line patients as well as in the second-line patients. As Dave explained, this arm is a pure Phase 1/2 with a single patient that went out to two prior lines of therapy. So having these data there, it's really going to allow us to plan and understand the activity in both of those settings. Thank you. Given we're seeing good disease stabilization across P1A so far, is the thinking that you see could act in a way that keeps cancer in check but doesn't necessarily cause it to shrink dramatically and therefore an increase in the max cumulative dose would allow for maintenance therapy? Yes, so progression-free survival, as we've noted, it's a very standard endpoint in oncology, and it's very meaningful. Patients really care most about how much time they have as opposed to how many millimeters did my tumor shrink by. And so given this, we're looking forward to its use in both the first line and the second line setting. Maintenance therapy, as mentioned here, has a little bit of a different connotation in oncology. A maintenance therapy is used only once a patient has developed a response to the drug, and they need to switch from the drug. The maintenance drug is designed to hold the response. But here, we're not requiring patients to develop a response. Even if they have just pure stable disease, it stops the growth. Those patients can then continue on FAP doxorubicin. And so the measurement that's made here is that 90% of patients fit into that disease control status. This reports that the vast majority of patients are seeing disease stabilization and not needing to develop that response. So we're very encouraged by the fact that the rate of 90% has held in that second cohort. Great. Thank you. We've got a two-part question here. Will enrollment continue in this cohort, and how many patients can we expect to see at the end of this phase of the trial? Yes, we do continue to enroll in this cohort. It's planned in the protocol for up to 30 patients. We may not include all of the 30 patients, and that's in addition to the 11 patients in the Phase 1A. We are continuing to look at each of these patients deeply, individually, from both clinical efficacy, safety, but also, as Ruairidh mentioned, we're looking at individual patients in terms of translational data. I can tell you definitively that, yes, additional patients will be added beyond the 19 that are available today. Thanks, Chris. This cohort includes more patients who have been treated in the first line setting. Why are we not seeing better efficacy data if that's the case here? The inclusion criteria for this cohort and the Phase 1A cohort are actually pretty similar. We didn't see any really deeply, heavily pretreated patients in the Phase 1A cohort. Nearing the end of that Phase 1A, we did actually amend the study to include patients who had not received prior therapy. There were a couple of patients in there that were treated in the first line setting. It is correct, however, that there are a few more patients in the first line setting in the Phase 1B cohort. It's important to note that these patients in general have been deemed to be chemorefractory. Salivary gland cancer, it's pretty much known to be a chemorefractory. We don't anticipate to see a very high response for this, let's call it specialized chemotherapy intervention. We're thrilled to see that the patients enrolled across lines appear to be seeing a similar efficacy of AVA6000. And we plan to continue enrollment for a small number of additional patients. And given the similarity of the two cohorts, we wouldn't necessarily expect to see a difference in efficacy. We are seeing, as we've reported previously, patients see efficacy after androgen deprivation therapy. They see efficacy after prior chemotherapy. And so we wouldn't expect to see a big difference between the first line and second line settings, which also leads to that we can do a mixed first line, second line Phase 2/3 trial. And so it really supports the design there. As we described previously, one level of clarity around that design, we are going to mix the first line and the second line setting. And so thus, the design needs to control the enrollment rates of each in the two arms. And so we think, given these data, it's worth taking on some of those complexities in the design. Great. Thanks, Chris. Is it max depletive of the dose selected for P1B? One question is whether you'd have gone higher or lower with the benefit of hindsight. Same question for TNBC, given this was dose selection and having dosed TNBC in P1A. Yeah, good question. And it really speaks to sort of how do you choose the recommended dose. So we are seeing preliminary safety from the expansion cohort, and that profile is holding up. We did see some challenging tolerability at the higher dose, the 385. And so backing down to the 310, we thought to make this a tolerable drug was important. We do continue to observe that in these patients, many of the toxicities associated with doxorubicin are associated with cumulative exposure. And so given that many of the patients are early, we may see some of those toxicities creep up. But importantly, given how early many of the patients are and many are still on therapy, we do have an evolving profile here, but we are very encouraged by the safety profile. The TNBC cohort, the triple negative cohort, is a bit of a challenge. One of the big differences here is that most of the patients are going to have been pretreated with an anthracycline such as doxorubicin. In their therapy, we call it adjuvant, so after they had their first surgery, and this complicates assessments. The patients are already going to be familiar with the potential toxicity profile here, so we are continuing to watch this cohort, and we are working with our investigators here to determine the appropriate dose in each of these disease settings. Thank you. There's a reference in a broker note to Avacta having conversations around potentially increasing the max cumulative dose equivalent to beyond 550 mg. Has the uplift from 450 mg to 550 mg seen much impact? And do we want to go higher than 550 mg if we're permitted? Yes. So let me take the first part of that. The change from 450 to 550 has had a meaningful impact. Patients can now receive approximately 20%-25% more drug than in the previous cohorts. And so that's a longer period of time that patients can be treated. And so to a patient who is responding to the drug and having that favorable safety profile, not needing to move on to the next regimen of combination chemo, to me, this represents an important change. It's a great question. We are looking to eliminate that lifetime maximum, but it is going to require agreement with the health authorities. And so while I can't comment on ongoing conversations with health authorities, what I can tell you is that the cardiac safety data, especially in patients stopping at the max of 550, these data were very favorable compared to conventional doxorubicin. This was something that we presented at ESMO. I can also commit to that once a decision is made, we will absolutely communicate this to the investigators, the patients, as well as to the shareholders alike. It is an important thing that we are looking at now. Great. Thank you. And comparing the endpoints of PFS and responses, how should we think about this disease stabilization versus shrinkage, especially since we don't necessarily see large decreases in tumor size? Yeah, it's a similar question, but it is important to reiterate. Although we are not seeing that high response rate, it's primarily because this disease setting is notorious for lack of responses. It's known to be chemorefractory. On the flip side, PFS as an endpoint is well accepted. I mean, it's one of the gold standard endpoints in oncology. It's the question that patients ask, "How long do I have?" In general, the survival endpoints in metastatic disease are considered to be the standards, and objective response rate is used as a surrogate endpoint for the survival endpoints that we see. I would say, having been a practicing oncologist, that while large decreases in tumor size are nice to have, they're really only meaningful when they're accompanied by an extension in survival. Many oncology drugs are approved based on PFS, and one can look no further than one of the more recent approvals in breast cancer. This is an ADC known as Trodelvy, which the primary endpoints were both survival endpoints. It was overall survival, and it was progression-free survival, and so I think that disease stabilization and for prolonged periods of time, progression-free survival is almost more important than seeing responses. We are seeing tumor shrinkage, and in general, it is accompanied, as Ruairidh mentioned in a few settings, it is accompanied by that prolonged disease stabilization or PFS, so we're excited about the data. We're highly encouraged that the Phase 1B looks to be right in line with the exciting data that we showed in the Phase 1A. Chris, thanks for answering those questions and updating investors today, and of course, I'm going to give you all questions submitted today, and we'll publish responses where appropriate to do so on the Investor Meet Company platform. Now, please ask investors not to close the session. It will be automatically redirected to provide your feedback in order that the management team could better understand your views and expectations. This will only take a few moments to complete, and it's greatly valued by the company. On behalf of the management team of Avacta Group PLC, we'd like to thank you for attending today's presentation, and good morning to you all.